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New treatments may be more effective against Alzheimer’s disease

In Alzheimer’s disease, proteins (peptides) form aggregates in the brain and the patient loses memory. In a recently published article, a research group at Uppsala University described a new treatment that increases the breakdown of the body itself in building blocks that lead to these protein clumps.

In Alzheimer’s disease, peptide amyloid beta begins to form aggregates in the brain. This process is called aggregation, and clamps created in this way are called aggregation. The treatment for Alzheimer’s disease, which is currently in clinical trials, is an attempt to bind to the aggregates that cause these diseases. However, they are unable to bind to the smallest aggregates and many now believe that they are the most toxic to neurons.

A treatment developed in a new Uppsala research study in mice breaks down the components that form these aggregates before they aggregate. Therefore, this treatment method reduces the formation of all types of agglomerates.

Could not be used in the past

The peptide somatostatin used by researchers in the Uppsala group has long been known to be able to activate the body’s own degradation of the amyloid beta, a peptide that forms aggregates. However, somatostatin was formed so far that it could not be used as a drug because it has a very short half-life in the blood of a few minutes and does not cross the blood-brain barrier to reach the brain where aggregates are present.

Therefore, in order to make somatostatin usable as a therapeutic drug, we fused it with a brain transport protein that allows somatostatin to enter the brain. This has proven to be very effective. Using transport proteins, we also found that somatostatin stayed in the brain for several days. This is great. “

Fadi Rofo, PhD student in the Faculty of Pharmaceutical and Biological Sciences, lead author of research

Maximum effect on hippocampus

In this study, researchers saw maximum effects in the hippocampus, the part of the brain that formed memory, and the first part affected by Alzheimer’s disease.

“The fact that it turned out to be most effective, especially in the hippocampus, is very good. I hope this method works in a very targeted way and has few side effects in question. “Other research,” said Greta Thunberg, an assistant professor in the Department of Pharmaceutical and Biological Sciences who led the research.

Although the study was conducted in mice, researchers believe that somatostatin has the same effect in humans and that this type of treatment is more effective than previously attempted.


Journal reference:

Rofo, F. , et al. (2020) Enhanced neprilysin-mediated degradation of hippocampal Aβ42 by somatostatin peptides that enter the brain. Ceranostics.

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